Myopia is an important public health problem due to its prevalence and significant public health cost. Elevating levels of myopia increase the risk of vision impairment, and therefore, high myopia has become one of the main causes of untreatable vision loss throughout the world due to its irreversible complications. At present, many options for slowing progression of myopia have already been proposed and evaluated such as progressive addition of executive bifocal spectacle lenses, peripheral defocusing lenses, overnight orthokeratology, pharmacological agents such as atropine eye drops, and multifocal soft contact lenses (MFSCLs). Use of MFSCLs has especially increased in recent years due to the growing demand to slow myopia progression during patient's adolescent growth period to avoid pathological myopia in adulthood. Compared with the other traditional methods of controlling myopia, MFSCLs allow myopic patients to better maintain their clear visual quality and slow myopia progression. In this manuscript, we aim to review the basics of myopia, recent advances in contact lenses to control myopia with emphasis on MFSCLs, define the elements for proper MFSCL fittings (such as pupil size, aberrations, accommodation and centering), discuss the potential rebound effect after discontinuation of contact lenses, and future directions for improvements of contact lenses for the control of myopia.

In this study, we aimed to investigate whether chronic retinal inflammation is involved in the pathogenesis of form-deprivation myopia (FDM) using tree shrews as an animal model. Twenty-one tree shrews were randomly divided into 7-day/14-day FDM (FDM7/FDM14) groups and their corresponding 7-day/14-day control groups. Refraction and axial length were measured. To determine the effects of form deprivation on inflammation, we used real-time polymerase chain reaction (PCR) and immunohistochemistry to assess the expression levels of several proinflammatory cytokines. At day 0, the eyes in the FDM and control groups were hyperopic. However, after 7 and 14 days of form deprivation, the refractive error of the eyes in the FDM7 and FDM14 groups shifted from +6.6 ± 0.3 diopters (D) to +4.0 ± 0.5 D and from +6.4 ± 0.3 D to +5.0 ± 0.3 D, respectively. The levels of tumor necrosis factor-α, interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1, and nuclear factor κB were increased in the FDM eyes, compared with those in the control eyes. The increase in matrix metalloproteinase-2 expression was greater in the FDM eyes than in the contralateral and control eyes, whereas collagen type I expression was downregulated. In conclusion, chronic inflammation may play a crucial pathogenic role in form-deprivation myopia in tree shrews.

Human corneal endothelial cells are responsible for controlling corneal transparency, however they are notorious for their limited proliferative capability. Thus, damage to these cells may cause irreversible blindness. Currently, the only way to cure blindness caused by corneal endothelial dysfunction is via corneal transplantation of a cadaver donor cornea with healthy corneal endothelium. Due to severe shortage of donor corneas worldwide, it has become paramount to develop human corneal endothelial grafts in vitro that can subsequently be transplanted in humans. Recently, we have reported effective expansion of human corneal endothelial cells by reprogramming the cells into progenitor status through use of p120-Kaiso siRNA knockdown. This new reprogramming approach circumvents the need of using induced pluripotent stem cells or embryonic stem cells. Successful promotion of this technology will encourage scientists to re-think how "contact inhibition" can safely be perturbed to our benefit, i.e., effective engineering of an in vivo-like tissue while successful maintaining the normal phenotype. In this review, we present current advances in reprogramming corneal endothelial cells in vitro, detail the methods to successful engineer human corneal endothelial grafts, and discuss their future clinical applications to cure corneal blindness.

Many neuropsychiatric disorders, such as schizophrenia, have been associated with olfactory dysfunction and abnormalities in the prepulse inhibition (PPI) response to a startle reflex. However, whether these two abnormalities could be related is unclear. The present investigations were designed to determine whether theblockage of olfactory sensory input by zinc sulfate infusion in the olfactory naris (0.5 ml, 0.17 M, ZnE) can disturb the PPI response. Furthermore, a bilateral microinjection of lidocaine/MK801 in the olfactory bulb (OB) was administered to examine whether the blockage of olfactory sensory input could impair the PPI response. To identify the neural projection between olfaction and PPI-related areas, trans-synaptic retrograde tracing with the recombinant pseudorabies virus (PRV) was used. Our results demonstrated that blockage of olfactory sensory input could disturb olfactory behavior. In the function studies, we demonstrated that blockage of olfactory sensory input could impair the pre-pulse inhibition of the startle response following decreased c-Fos expression in relevant brain regions during the PPI responses. Furthermore, similar and more robust findings indicated that blockage of olfactory sensory input by microinjection of lidocaine/MK801 in the OB could impair the PPI response. In the circuit-level studies, we demonstrated that trans-synaptic retrograde tracing with PRV exhibited a large portion of labeled neurons in several regions of the olfactory cortices from the pedunculopontine tegmental nucleus (PPTg). Thus, these data suggest that the olfactory system participates in the PPI regulating fields and plays a role in the pre-pulse inhibition of the startle response in rats.